A pilot observational study on magnesium and calcium imbalance in elderly patients with acute aortic dissection
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RESEARCH
Open Access
A pilot observational study on magnesium and calcium imbalance in elderly patients with acute aortic dissection E. Vianello1*, E. Dozio1, A. Barassi2, G. Sammarco3, L. Tacchini1, M. M. Marrocco-Trischitta4, S. Trimarchi1,4 and M. M. Corsi Romanelli1,3
Abstract Background: Magnesium (Mg) and calcium (Ca) are the principal essential elements involved in endothelial cell homeostasis. Extracellular changes in the levels of either alter endothelial contraction and dilatation. Consequently Mg and Ca imbalance is associated with a high risk of endothelial dysfunction, the main process observed during acute aortic dissection (AAD); in this clinical condition, which mainly affects elderly men, smooth muscle cell alterations lead to intimal tears, creating a false new lumen in the media of the aorta. AAD patients have a high risk of mortality as a result of late diagnosis because often it is not distinguished from other cardiovascular diseases. We investigated Mg and Ca total circulating levels and the associated pro-inflammatory mediators in elderly AAD patients, to gain further information on the pathophysiology of this disorder, with a view to suggesting newer and earlier potential biomarkers of AAD. Results: Total circulating Mg and Ca levels were both lower in AAD patients than controls (p < 0.0001). Using Ca as cut-off, 90% of AAD patients with low Ca ( 0.05) The levels of both ICAM-1 and EN-1 were lower in AAD than in a control group (p < 0.0001 and p < 0.05 respectively). Conclusions: These findings suggest that low Mg and Ca in AAD elderly patients may contribute to altering normal endothelial physiology and also concur in changing the normal concentrations of different mediators involved in vasodilatation and constriction, associated with AAD onset and severity. Keywords: Magnesium (Mg), Calcium (Ca), Acute aortic dissection (AAD)
Background Magnesium (Mg) and calcium (Ca) are involved in the most essential processes regulating cardiovascular function and their imbalance is a factor in the development of numerous disorders of the cardiovascular system, mostly linked to endothelial dysfunction and inflammation, mainly affecting vascular smooth muscle cells (VSMCs) [1]. In humans and animals extracellular Mg * Correspondence: [email protected] 1 Department of Biomedical Sciences for Health, Chair of Clinical Pathology, Università degli Studi di Milano, via Luigi Mangiagalli 31, 20133 Milan, Italy Full list of author information is available at the end of the article
has cardioprotective properties because it attenuates all the agonist-induced vasoconstriction molecules, including endothelin-1 (EN-1), helping preserve vascular tone and preventing coronary vasospasm [1–5]. These cardioprotective effects are reinforced by the fact that Mg assists the coagulation reactions, binding specific coagulation proteins in case of endothelial damage [6]. In the cardiovascular system, one of the main mechanisms that regulates VSMC activity during pressure load is the Ca channel block mediated by Mg
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